Obesity and Arterial Stiffness

Long-term follow-up studies have indicated that obesity is a predictor
of cardiovascular risk in both genders. Obesity is the culprit behind heart ailments like hypertension, heart attack, high cholesterol and coronary artery disease.

Obesity and Arterial Stiffness

Arterial stiffening occurs as we age and is is associated with an increased risk of cardiovascular diseases like Stroke and myocardial infarction. The gold standard method to check arterial stiffness is by measuring the carotid femoral pulse wave velocity. Increased arterial stiffness is reflected by an increased pulse wave velocity (PWV) and is generally seen to be associated with higher risk for cardiovascular morbidity and mortality.

Recently in the past few years it has been demonstrated that individuals with obesity are likely to have an increased aortic stiffness which predisposes them to risk for cardiovascular diseases. This is independent of Blood pressure level, ethnicity, and age.

Though the pathophysiologic mechanisms that link abdominal adiposity to stiffening are not fully understood, several mechanisms have been cited.

· Visceral adipocytes
have an elevated lipolytic activity that results in increased free fatty acids
release in the portal vein with an accumulation (liver, pancreas, and muscles)
that contributes to insulin resistance.

· Other mechanisms such
as increases in circulating pro-inflammatory cytokines or leptin. High levels
of leptin have been documented in individuals with obesity and found to be
correlated with reduction in arterial distensibility.

· In addition, leptin
induces oxidative stress in endothelial cells, and this action triggers the
transcription of oxidant-sensitive genes that participate in atherogenesis.

· Leptin increases sympathetic nervous activity. It is possible that the high levels of leptin
that are observed in obesity could contribute to its adverse effects on cardiovascular health.

· Increase in circulating pro-inflammatory cytokines may contribute to the development of cardiovascular disease in obese individuals.

· The reduced arterial elasticity may be the consequence of hyperglycemias and/or insulin's acting either directly or through the development of advanced glycation end products. Non-enzymatic glycosylation of the matrix proteins of arterial vessels may enhance the production of cross-links between collagen fibers, which in turn could cause arterial stiffness and systolic hypertension.

All the above reasons could be attributed to arterial stiffening in an obese
individual.

In a recent study published on bio-medcentral, it was found that most measures of obesity like the Body Mass Index, Waist circumference, Waist to hip ratio or the visceral fat are strong predictors of arterial stiffness. These can also be used to asses ones risk to arterial stiffening and cardiovascular disease risk.

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